Fig. 1.
Ketamine (Ket) had no effect on synaptic γ-aminobutyric acid (GABA) currents but increased the currents evoked by low concentrations of GABA in hippocampal neurons. (A) Representative recordings of GABA receptor type A (GABAA) receptor–mediated miniature inhibitory postsynaptic currents (mIPSCs) from the same neuron, before and during application of ketamine. (B) Traces were averaged from 557 (control) and 522 (ketamine) individual mIPSCs. (C) Cumulative distributions of the amplitude (left) and frequency (right) of mIPSCs showing that both the amplitude and frequency were not affected by ketamine. P = 0.07 for the amplitude, P = 0.12 for the frequency, Kolmogorov−Smirnov test. (D) Representative traces and summarized data showing that current evoked by GABA (0.3 μM) was increased by ketamine. Two-way ANOVA, effect of ketamine treatment: F(1,54) = 121.1, P < 0.0001; effect of ketamine concentration: F(3,54) = 3.6, P = 0.03; effect of interaction: F(3,54) = 27.4, P < 0.0001; n = 6 for 10 μM ketamine, n = 9 for 30 μM ketamine, n = 8 for 100 and 300 μM ketamine, ***P < 0.001 compared with control, Bonferroni post hoc test. (E) Summarized data showing the effects of ketamine (300 μM) on currents evoked by different concentrations of GABA. Two-way ANOVA, effect of ketamine treatment: F(1,44) = 27.3, P < 0.0001; effect of GABA concentration: F(2,44) = 137.3, P < 0.0001; effect of interaction: F(2,44) = 3.3, P = 0.06; n = 8 for 0.3 and 0.5 μM GABA, n = 9 for 10 μM GABA, *P < 0.05, ***P < 0.001 compared with control, Bonferroni post hoc test.

Ketamine (Ket) had no effect on synaptic γ-aminobutyric acid (GABA) currents but increased the currents evoked by low concentrations of GABA in hippocampal neurons. (A) Representative recordings of GABA receptor type A (GABAA) receptor–mediated miniature inhibitory postsynaptic currents (mIPSCs) from the same neuron, before and during application of ketamine. (B) Traces were averaged from 557 (control) and 522 (ketamine) individual mIPSCs. (C) Cumulative distributions of the amplitude (left) and frequency (right) of mIPSCs showing that both the amplitude and frequency were not affected by ketamine. P = 0.07 for the amplitude, P = 0.12 for the frequency, Kolmogorov−Smirnov test. (D) Representative traces and summarized data showing that current evoked by GABA (0.3 μM) was increased by ketamine. Two-way ANOVA, effect of ketamine treatment: F(1,54) = 121.1, P < 0.0001; effect of ketamine concentration: F(3,54) = 3.6, P = 0.03; effect of interaction: F(3,54) = 27.4, P < 0.0001; n = 6 for 10 μM ketamine, n = 9 for 30 μM ketamine, n = 8 for 100 and 300 μM ketamine, ***P < 0.001 compared with control, Bonferroni post hoc test. (E) Summarized data showing the effects of ketamine (300 μM) on currents evoked by different concentrations of GABA. Two-way ANOVA, effect of ketamine treatment: F(1,44) = 27.3, P < 0.0001; effect of GABA concentration: F(2,44) = 137.3, P < 0.0001; effect of interaction: F(2,44) = 3.3, P = 0.06; n = 8 for 0.3 and 0.5 μM GABA, n = 9 for 10 μM GABA, *P < 0.05, ***P < 0.001 compared with control, Bonferroni post hoc test.

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